Atrial Flutter

Atrial Flutter


The CTI is the region of right atrial tissue bounded posteriorly by the IVC and anteriorly by the tricuspid annulus forming a protected zone of slow conduction that plays a critical role in CTI-dependent flutter. The CTI can be divided into three sections: septal, central (6 o’clock on LAO view), and inferolateral isthmus.5 The thicker paraseptal isthmus is bounded by the coronary sinus (CS) os and thick eustachian ridge and closer to the right inferior extension of the atrio-ventricular (AV) node and AV nodal artery. The inferolateral isthmus is the longest, contains pectinate muscles of the terminal crest, and is closest endocardially to the right coronary artery. The central isthmus is the shortest and thinnest but a potential site for pouch-like recesses. CTI ablation involves creation of a line of block (LOB) across the isthmus by a series of coalescing ablation lesions that connect the 1) tricuspid annulus to the IVC (posterior line transecting the central or inferolateral isthmus) or 2) tricuspid annulus to CS os—CS os to eustachian ridge/valve (septal line transecting the paraseptal isthmus with the eustachian ridge/valve serving as a LOB between the CS os and IVC).2,3,4,6 Because the septal line is associated with a higher risk of AV block and traverses the thick muscular eustachian ridge making ablation difficult, a posterior line (particularly transecting the shorter, thinner central isthmus) is preferred as the initial target for ablation.5,7



The circuit for CCW CTI-dependent flutter is confined to the right atrium (RA) with lateral to medial conduction across the isthmus (Fig. 14-2). The CCW activation wavefront exits the medial end of the CTI near the CS os, ascends the interatrial septum, depolarizes the roof of the RA, and then descends along the anterolateral right atrial wall before depolarizing the lateral CTI. The left atrium is passively activated and not an integral

part of the circuit. Several anatomic barriers prevent a short circuit of the reentrant pathway and include the 1) tricuspid annulus (anterior barrier); 2) IVC, eustachian ridge (medially), and crista terminalis (laterally) (posterior barriers); 3) and endocardial cavity of the RA.6,8,9 The circuit for CW CTI-dependent atrial flutter is the reverse of its typical counterpart with medial to lateral activation of the CTI (Fig. 14-3).

FIGURE 14-1 CCW CTI (top) and mitral isthmus (bottom) flutter. Note the “early meets late” pattern in the right and left atrium, respectively, with passive activation of the counterpart chamber.

FIGURE 14-2 CCW CTI-dependent atrial flutter. Note the “early meets late” pattern (white/purple interface) with CCW activation around the tricuspid annulus.


12-Lead ECG

The classic CCW CTI-dependent atrial flutter is 1) positive in V1; 2) negative in II, III, aVF (“sawtooth” pattern); and 3) absent isoelectric line (except in V1) (V1/II discordance) (Fig. 14-4). The downslope, nadir, and upslope of the “sawtooth” flutter wave correspond to ascending activation of the interatrial septum, depolarization of the right atrial roof, and descending activation of the anterolateral free wall, respectively. Location of the isthmus exit site at the posteroseptum near the CS os creates an anteriorly directed flutter vector and, therefore, slightly positive flutter waves in V1. Continuous activation of the RA that spans the entire flutter cycle length causes absence of an isoelectric interval between flutter waves. CW CTI-dependent atrial flutter is opposite of its CCW counterpart: 1) negative in V1 and 2) positive in II, III, and aVF (often with notching) (V1/II discordance) (Fig. 14-4). Atrial flutter showing V1/II concordance (e.g., positive in V1 and II) indicates a non-CTI-dependent flutter (e.g., left atrial flutter).

Electrophysiologic Study

Demonstrating CCW and CW activation around the tricuspid annulus during CTI-dependent flutter involves mapping the RA with multipolar recording catheters: anterolateral RA and CTI (“Halo” catheter), 2) CS os (posteroseptum), and 3) His
bundle (anteroseptum) or a three-dimensional electro-anatomic mapping system. CCW CTI-dependent flutter is more readily induced by burst pacing than programmed extrastimulation, particularly from the smooth (medial) RA where pacing can induce medial to lateral block (unidirectional block) across the CTI (Fig. 14-5). Pacing from the trabeculated (lateral) RA induces CW CTI-dependent flutter.10

FIGURE 14-3 CW CTI-dependent atrial flutter. Note the “early meets late” pattern (white/purple interface) with CW activation around the tricuspid annulus.


CTI dependency is determined by the response of atrial flutter to entrainment from the CTI (Fig. 14-6).8,9 Delivery of pacing stimuli from the CTI at a cycle length 10-30 ms shorter than the flutter cycle length captures the atrium and penetrates its excitable gap, giving rise to orthodromic and antidromic wavefronts. The antidromic wavefront of the first stimulus (n) collides with tachycardia. Its orthodromic counterpart exits the isthmus, advances the atrium in the direction of tachycardia, and collides with the antidromic wavefront of the next pacing stimulus (n + 1). Each n orthodromic wavefront collides with the n + 1 antidromic wavefront until pacing stops. The last orthodromic wavefront has no antidromic wavefront with which to collide and completes one revolution around the circuit followed by continuation of atrial flutter. The post-pacing interval (PPI) (measured from the last pacing stimulus to the first atrial electrogram on the pacing catheter) equals the atrial flutter cycle length. The following criteria demonstrate CTI dependency with entrainment from the CTI: 1) concealed ECG fusion, 2) St-flutter wave = egm − flutter wave, and 3) PPI − atrial flutter cycle length ≤20 ms (Fig. 14-6). While surface ECG flutter morphology during entrainment and tachycardia are identical, intracardiac fusion occurs as a result of antidromic capture “upstream” to the pacing site. A PPI – atrial flutter cycle length >20 ms suggests a non-CTI-dependent flutter unless rate-dependent conduction delay within the circuit produces a long PPI (Fig. 14-7).11

FIGURE 14-4 A 12-lead ECG of CCW and CW CTI-dependent atrial flutter. Note the discordant polarity of the atrial flutter waves in V1 and inferior leads. Top: Atrial flutter waves are positive in V1 and negative (“saw tooth”) inferiorly. Bottom: Atrial flutter waves are negative in V1 and positive inferiorly. Both ECGs also show grouped QRS beating (alternating Wenckebach periodicity) due to two levels of AV block (upper level: 2:1; lower level: Wenckebach).



The CTI has a defined anatomic location, and ablation can be performed either during sinus rhythm (CS pacing) or atrial flutter.12,13 Ongoing flutter, however, allows both entrainment and termination to prove CTI dependency. The ablation catheter is positioned at the annular end of the CTI where small atrial and large ventricular electrograms are recorded. Radiofrequency (RF) energy is delivered in a point by point (“spot welding”) or continuous (“drag”) fashion as the catheter is pulled back across the floor of the CTI from annular to caval end. Effective lesions are indicated by voltage abatement and

loss of sharp, high-frequency content (often accompanied by referred pain to the right shoulder). RAO fluoroscopy estimates the degree of posterior catheter movement along the CTI, while the LAO view reveals medial or lateral drift of the catheter from the ablation line.

FIGURE 14-5 Induction of CCW CTI-dependent atrial flutter by an APC (asterisk) (top) and rapid atrial pacing (bottom). In both cases, medial to lateral CTI block (“unidirectional block”) followed by CCW activation around the tricuspid annulus (“slow conduction”) initiates macroreentry.

FIGURE 14-6 Entrainment of CCW (top) and CW (bottom) CTI-dependent atrial flutter from the CTI. In both cases, entrainment with concealed fusion and PPI ≈ TCL (<20 ms) indicate CTI dependency.

FIGURE 14-7 Entrainment of CCW CTI-dependent atrial flutter with progressive fusion and long PPI. Top: At a pacing cycle length of 340 ms, entrainment results in constant concealed fusion, the last orthodromically entrained electrograms occurring at the pacing cycle length (electrograms downstream to the point of orthodromic/antidromic collision [RA 4 and 5]), and PPI = TCL (first criteria of transient entrainment). A faster pacing cycle length of 290 ms results in progressive fusion (greater antidromic capture from the pacing site with the collision point shifted upstream [RA 6 and 7]) and PPI − TCL = 39 ms.

During Atrial Flutter

Successful CTI ablation results in cycle length slowing and/or termination of CTI-dependent flutter. The last recorded atrial electrogram is immediately upstream to the ablation line (Figs. 14-8, 14-9, 14-10 and 14-11).

FIGURE 14-8 Termination of CCW CTI-dependent atrial flutter by ablation. Note the catheter inversion technique to target the thick posterior eustachian ridge. Red tags denote ablation lesions across the CTI.

FIGURE 14-9 Termination of CCW CTI-dependent atrial flutter by ablation. Atrial flutter breaks in the CTI at the ablation line confirming isthmus dependency.

FIGURE 14-10 Termination of CCW CTI-dependent atrial flutter by ablation. Atrial flutter breaks in the CTI at the ablation line confirming isthmus dependency.

FIGURE 14-11 Termination of CW CTI-dependent atrial flutter by ablation. Atrial flutter breaks in the CTI at the ablation line confirming isthmus dependency.

Oct 13, 2019 | Posted by in CARDIOLOGY | Comments Off on Atrial Flutter

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